نتایج جستجو برای: copd mice model
تعداد نتایج: 2448346 فیلتر نتایج به سال:
BACKGROUND Chronic obstructive pulmonary disease (COPD) is characterized by excessive inflammation and disturbed bacterial clearance in the airways. Although cigarette smoke (CS) exposure poses a major risk, vitamin D deficiency could potentially contribute to COPD progression. Many in vitro studies demonstrate important anti-inflammatory and antibacterial effects of vitamin D, but a direct con...
Over the last decade, a previously unknown role has been established for members of the C/EBP transcription factor family in lung gene expression. In other organs, C/EBPs are well known regulators of cell differentiation and linked processes such as proliferation, apoptosis, gene expression as well as central regulators of inflammatory responses and infectious defenses. The scope of this thesis...
purpose: the purpose of this study is to model cryptosporidiosis in laboratory animals. the parasites were inoculated into animalsand thenmultiplied. the process of proliferation was compared to controlcryptosporidiosis in humans. materials and methods: twenty-five laboratory mice (4-7 days of age) and twenty-five laboratory rats (5 days of age) were assigned to the category i while the categor...
Inducible NOS Inhibition Reverses Tobacco-Smoke-Induced Emphysema and Pulmonary Hypertension in Mice
Chronic obstructive pulmonary disease (COPD) is one of the most common causes of death worldwide. We report in an emphysema model of mice chronically exposed to tobacco smoke that pulmonary vascular dysfunction, vascular remodeling, and pulmonary hypertension (PH) precede development of alveolar destruction. We provide evidence for a causative role of inducible nitric oxide synthase (iNOS) and ...
مقدمه: در تعریف شخصیت آمده است ویژگی های نسبتاً پایدار فرد که در نحوه رفتاری وی در شرایط مختلف تظاهر می کند طبق نظریه کلونینجر شخصیت از دو بعد سرشت و منش تشکیل شده است که عوامل مختلفی باعث تغییر در ویژگی های منش و تعدیل ویژگی های سرشت می شود. copd (بیماری انسدادی مزمن ریوی) به عنوان یک بیماری که به وسیله ی محدودیت جریان هوا که به طور کامل برگشت پذیر نمی باشد، معرفی شده است هدف از مطالعه ما بررسی...
Viral exacerbations of chronic obstructive pulmonary disease (COPD), commonly caused by rhinovirus (RV) infections, are poorly controlled by current therapies. This is due to a lack of understanding of the underlying immunopathological mechanisms. Human studies have identified a number of key immune responses that are associated with RV-induced exacerbations including neutrophilic inflammation,...
INTRODUCTION Chronic obstructive pulmonary disease (COPD) is a progressive disorder that makes the breathing difficult and is characterized by pathological conditions ranging from chronic inflammation to tissue proteolysis. With regard to ethical issues related to the studies on patients with COPD, the use of animal models of COPD is inevitable. Animal models improve our knowledge about the bas...
Chronic obstructive pulmonary disease (COPD) is a debilitating disease caused by chronic exposure to cigarette smoke (CS), which involves airway obstruction and alveolar loss (i.e., emphysema). The mechanisms of COPD pathogenesis remain unclear. Our previous studies demonstrated elevated autophagy in human COPD lung, and as a cellular and tissue response to CS exposure in an experimental model ...
Smoking is the main risk factor for the development of the chronic obstructive pulmonary disease (COPD) in Western countries. Recent studies suggest that IL-17A and Th17 cells play a role in the pathogenesis of COPD. We used a murine model of chronic cigarette smoke (CS) exposure to explore the contribution of IL-17A to CS-induced lung damage and loss of pulmonary function. Histology and morpho...
BACKGROUND Decreased activity of forkhead transcription factor class O (FoxO)3A, a negative regulator of NF-κB-mediated chemokine expression, is implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). Previously, we showed that quercetin reduces lung inflammation in a murine model of COPD. Here, we examined the mechanisms underlying decreased FoxO3A activation and its mo...
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